Mac-1-mediated Uptake and Killing of Bordetella bronchiseptica by Porcine Alveolar Macrophages.
- Author:
Jong Keuk LEE
1
;
Lawrence B SCHOOK
;
Mark S RUTHERFORD
Author Information
1. National Genome Research Institute, National Institute of Health, 5 Nokbun-dong, Eunpyung-ku, Seoul 122-701, Korea. cookie_jklee@hotmail.com
- Publication Type:Original Article
- Keywords:
Mac-1;
Bordetella bronchiseptica;
alveolar macrophage;
pig
- MeSH:
Animals;
Antibodies, Bacterial/blood/immunology;
Bordetella bronchiseptica/*immunology;
Macrophage-1 Antigen/*immunology;
Macrophages, Alveolar/*immunology;
Phagocytosis;
Protein Binding;
Swine/*immunology/*microbiology
- From:Journal of Veterinary Science
2003;4(1):41-49
- CountryRepublic of Korea
- Language:English
-
Abstract:
The role of Mac-1 as a receptor for Bordetella bronchiseptica infection of alveolar macrophages (AMphi) was examined using 6 strains (2 ATCC and 4 pathogenic field isolates) to assess B. bronchiseptica binding, uptake and replication in primary porcine AMphi. All B. bronchiseptica strains were rapidly killed by porcine serum in a dose- and time-dependent manner. However, heat-inactivated porcine serum (HIS) did not demonstrate any bacterial-killing activity, suggesting that complement may have a direct killing activity. All field isolates were more resistant to direct complement-mediated B. bronchiseptica killing. The uptake of B. bronchiseptica into AMphi was inhibited approximately 50% by antiMac-1 monoclonal antibodies in the medium. However, B. bronchiseptica phagocytosed in the presence of serum or HIS was not altered by anti-Mac-1 antibodies although more bacteria were internalized by addition of serum or HIS. These data suggest that Mac-1 is a target for direct uptake of B. bronchiseptica via opsoninindependent binding. The phagocytosed B. bronchiseptica, either via direct or serum-mediated binding, were efficiently killed by AMphi within 10 hr postinfection. This demonstrates that Mac-1-mediated B. bronchiseptica uptake is a bacterial killing pathway not leading to productive infections in AMphi.
